Tau is definately as important as Abeta as a preventive and therapeutic target for AD although paying too much attention to phoshphorylation is likely to be misleading for the following reason. The observations demonstrating that the PHF tau proteins in transgenic mice overexpressing FTDP-17 mutation-carrying tau are also highly phosphorylated seem to logically imply to me that phosphorylation is more likely to be a consequence, possibly of neurons struggling to protect themselves, rather than a cause of NFT formation, unless the mutations exert their effects through altering the phosphorylation/dephosphorylation status of tau, which has never been demonstrated to my knowledge.
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RIKEN Center for Brain Science
Tau is definately as important as Abeta as a preventive and therapeutic target for AD although paying too much attention to phoshphorylation is likely to be misleading for the following reason. The observations demonstrating that the PHF tau proteins in transgenic mice overexpressing FTDP-17 mutation-carrying tau are also highly phosphorylated seem to logically imply to me that phosphorylation is more likely to be a consequence, possibly of neurons struggling to protect themselves, rather than a cause of NFT formation, unless the mutations exert their effects through altering the phosphorylation/dephosphorylation status of tau, which has never been demonstrated to my knowledge.
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